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At least 19 recordsLinked to original sources
PubMed1993

Immunohistochemistry detects differences between lichen planus-like keratosis, lichen planus, and lichenoid actinic keratosis.

Lichen planus-like keratosis (LPLK) (benign lichenoid keratosis) is a common skin lesion that shows some morphologic features of lichen planus (LP) and lichenoid actinic keratosis (LAK). To try to detect differences among these three entities, immunohistochemical staining for S100 protein and HLA-DR (with the antibody LN3) was performed in 31 cases of LPLK, 26 of LAK, and 25 of LP. Langerhans cells (LC) were counted per linear mm of epidermis in the S100 and LN3 slides. With anti-S100 staining, LP cases showed higher numbers of LC (mean = 25.3, SE = 2.84, median = 21.2) than did LPLK (mean = 17.3, SE = 2.26, median = 14.5) and LAK (mean = 9.7, SE = 1.5, median = 5.4). With LN3 stains, LP cases also showed higher numbers of LC than did LPLK and LAK. These results suggest that the involvement of LC in the production of lesions may be different in these three entities. However, due to the overlap in distribution of values observed, the use of these stains does not allow a definite diagnosis to be made exclusively based on the number of LC.

Adult↗
PubMed1990

Hereditary palmoplantar keratosis of the Gamborg Nielsen type. Clinical and ultrastructural characteristics of a new type of autosomal recessive palmoplantar keratosis.

A new kind of diffuse palmoplantar keratoderma with autosomal recessive inheritance and without associated symptoms was described in Norrbotten, Sweden by Gamborg Nielsen in 1985. Clinically, it ranges between the less severe dominant Unna-Thost type and the more severe recessive Meleda type, as it is milder than the latter. Skin biopsies of five patients from three different families with this new palmoplantar keratoderma, as well as five obligatory heterozygotes from one family, were investigated ultrastructurally in order to characterize this new entity and to differentiate it from the Meleda type. Several features are common to both autosomal recessive palmoplantar keratoses. They show a broadened granular layer, a transit region consisting of cells with a marginal envelope, and considerable hyperkeratosis. Morphologically, this transformation delay is less pronounced in the Gamborg Nielsen type than in the classical Meleda type. As is typical for ridged skin, both types of palmoplantar keratoses possess composite keratohyaline granules. In contrast to the normal appearance of keratohyaline granules in the Meleda type, the Gamborg Nielsen type also shows qualitative deviations of keratohyaline granules with different degrees of spongiosity and electron density and sometimes with a granular border. It seems that abnormal keratohyaline proteins are synthesized that behave differently. The sudden transformation of a granular into a horny cell is physiologically regulated by different enzymes. A delay in this process may be caused by a mutation that reduces or alters the enzymes concerned. We assume the palmoplantar keratoderma of the Gamborg Nielsen type to be a variant of the heterogeneous group of the Meleda type of palmoplantar keratoderma with autosomal recessive inheritance.

Female↗
PubMedDate not supplied

[Environmental and occupational risk factors in keratosis of the larynx].

Laryngeal keratosis may frequently precede the appearance of carcinoma of the larynx which might well indicate that these diseases have a common denominator. A retrospective study of 120 subjects with laryngeal keratosis was examined. The intention of the Authors was to verify whether the principle risk factors involved in the appearance of laryngeal carcinoma were the same as those implicated in laryngeal keratosis formation. Sex age, work activity, cigarette smoke, alcohol consumption and vocal chord abuse were considered. Laryngeal keratosis takes keratosis with dysplasia as well as keratosis without. A link between these two types of keratosis and cancer was sought. In particular, the possibility that a persistent action of the mentioned risk factors could cause laryngeal dysplasia-free keratosis to change into dysplastic lesions and subsequently into cancer was investigated. A case-control study was performed in order to analyze the importance of work activity. Results were statistically significant (P < 0.001). The Cramer V2 calculation demonstrated a clear correlation between the number of cigarettes smoked and the appearance of dysplasia (V2 = 0.117; P < 0.005). Results showed a clearly different behaviour between sexes. The number of males was much higher than females as was the age at which keratosis appeared greater in males. The fact that the average age in which keratosis appeared preceded the appearance of laryngeal cancer by ten years indicates that this interrum is sufficient for keratosis with dysplasia to be transformed into cancer (due to the continued action of the mentioned etiologic factors, mainly referred to cigarette smoke). In our data analysis, no correlation was demonstrated between keratosis without dysplasia and cancer.

Adolescent↗
PubMed1994

The relationship between basal cell epithelioma and seborrheic keratosis. A study of 60 cases.

BACKGROUND: Various skin tumors can be seen rarely in association with seborrheic keratosis. We present 60 cases of seborrheic keratosis related to a basal cell epithelioma in the same specimen. OBJECTIVE: To report association of basal cell epithelioma with seborrheic keratosis and discuss the possibility of malignant change in seborrheic keratosis. METHODS: Sixty cases of seborrheic keratosis associated with basal cell epithelioma were studied. Tissues were fixed in neutral buffered formalin, processed, and stained with standard hematoxylin and eosin techniques. RESULTS: Histological evaluation showed a seborrheic keratosis associated with basal cell epithelioma in all of the cases. Basal cell epithelioma was attached with seborrheic keratosis in a majority of the cases (40/60) and appeared to represent a part of the same tumor. Both tumors were lying adjacent to each other in the rest of the cases (20/60). CONCLUSION: Malignant change in seborrheic keratosis is controversial. We recommend the histological evaluation of seborrheic keratosis especially when inflamed or atypical in appearance. This should not be taken as a mandate for pathological evaluation or for treatment of every seborrheic keratosis as though it was potentially malignant.

Adult↗
PubMed2002

Prevalence of melanoma clinically resembling seborrheic keratosis: analysis of 9204 cases.

OBJECTIVE: To estimate the prevalence of melanoma clinically mimicking seborrheic keratosis. DESIGN: Retrospective review of cases submitted for histological examination with a clinical diagnosis of seborrheic keratosis or with a differential diagnosis that included seborrheic keratosis. SETTING: A tertiary medical care center-based dermatopathology laboratory serving academic dermatology clinics that have a busy pigmented lesion clinic. MATERIALS AND METHODS: A total of 9204 consecutive pathology reports containing a diagnosis of seborrheic keratosis in the clinical information field were identified between the years 1992 and 2001 through a computer database search. Reports with a final histological diagnosis of melanoma were selected for further review and clinicopathological analysis. MAIN OUTCOME MEASURE: Histological diagnosis, which was correlated with the preoperative clinical diagnosis. RESULTS: Melanoma was identified in 61 cases (0.66%) submitted for histological examination with a clinical diagnosis that included seborrheic keratosis. Melanoma was in the clinical differential diagnosis of 31 cases (51%). The remaining lesions had a differential diagnosis of seborrheic keratosis vs melanocytic nevus (17 cases, 28%), basal cell carcinoma (7 cases, 12%), or a squamous proliferation (3 cases, 5%). In 3 cases (5%), seborrheic keratosis was the only clinical diagnosis. All histological types of melanoma were represented. CONCLUSIONS: Our results confirm that melanoma can mimic seborrheic keratosis. These data strongly support the current policy of submitting for histological examination all specimens that have been removed from patients.

Adult↗
PubMed2002

Pagetoid variant of actinic keratosis with or without squamous cell carcinoma of sun-exposed skin: a lesion simulating extramammary Paget's disease.

BACKGROUND: Extramammary Paget's disease usually occurs in anogenital skin. We present five cases of squamous cell carcinoma in situ of sun-exposed skin and non-squamous cell carcinoma in situ actinic keratosis that displayed atypical keratinocytes disposed in intraepithelial cell nests and immunohistochemical staining simulating extramammary Paget's disease. METHODS AND RESULTS: Two pilot cases--one squamous cell carcinoma in situ and one non-squamous cell carcinoma in situ actinic keratosis with formation of intra-epidermal nests of atypical keratinocytes with a pagetoid spread pattern--were encountered at our institution. Fifty-four consecutive cases of squamous cell carcinoma in situ including bowenoid actinic keratosis and 34 cases of non-squamous cell carcinoma in situ actinic keratosis were reviewed to identify pagetoid spread of atypical cells. Representative sections of all cases with pagetoid spread of atypical keratinocytes were submitted for special stains for mucin, and immunostaining for cytokeratin 7 (CK7), cytokeratin 20 (CK20), cytokeratin CAM 5.2 (CAM 5.2), carcinoembryonic antigen (CEA), vimentin and S100 protein. In the group of squamous cell carcinoma in situ, 10 cases displayed pagetoid spread of atypical keratinocytes with cytoplasm ranging from clear to pale and atypical hyperchromatic nuclei. One review squamous cell carcinoma in situ was multicentric with three separate lesions. The atypical keratinocytes tended to form well to poorly defined cell groups extending from the basal cell layer to the corneal layer. No similar cases were identified in the group of non-squamous cell carcinoma in situ actinic keratosis. Two pilot cases and three of 10 review cases with a total of seven separate lesions displayed a moderate to marked immunohistochemical reactivity for CK7 similar to extramammary Paget's disease. CEA immunoreactivity was also detected in two of these cases. In addition, two of 44 squamous cell carcinomas in situ without pagetoid spread of atypical keratinocytes showed a moderate reactivity for CK7 in very occasional atypical keratinocytes. The remaining seven squamous cell carcinomas in situ with pagetoid spread of atypical keratinocytes were not immunoreactive for CEA and CK7. Immunostaining for CK20, vimentin, S100 protein was negative in all atypical cells in all study cases. CONCLUSIONS: Actinic keratosis, particularly squamous cell carcinoma in situ of sun-exposed skin, may have histopathological and immunohistochemical features similar to extramammary Paget's disease and probably represents a variant of actinic keratosis. Awareness of the pagetoid variant of actinic keratosis arising in sun-exposed skin is helpful to avoid the over-diagnosis of extramammary Paget's disease.

Adult↗
PubMed1997

A possible case of eccrine poroma arising in seborrheic keratosis with partial intermediate malignancy and tumor of the follicular infundibulum.

An eighty-year-old woman presented with a eccrine poroma that appeared to have arisen in a seborrheic keratosis lesion on the right side of her abdomen. The tumor consisted of a brownish, flat, elevated lesion with an eroded nodule at its periphery. Histopathological analysis of the flat, elevated lesion revealed benign basaloid and squamoid cells that showed acanthotic upward proliferation, suggesting a seborrheic keratosis. The eroded nodule showed irregular proliferation of slight atypical squamoid cells with, in parts, ductal structures in the upper dermis, suggesting that it was an eccrine poroma with partial intermediate malignancy. In addition to the eroded nodule, an occult tumor clinically accompanied the seborrheic keratosis. Histopathology of the occult tumor revealed fenestrated columns and cords of pale epithelial cells attached to the base of the seborrheic keratosis lesion, which was diagnosed as a tumor of the follicular infundibulum. Although reports of seborrheic keratosis transforming into a sweat gland tumor are rare, the present case suggests that seborrheic keratosis may develop into benign or malignant adnexal tumors, including sweat gland and follicular tumors. Thus, seborrheic keratosis should be considered as a possible precursor of adnexal tumor.

Aged↗
PubMed2001

Comparative histochemical study of Bowen's disease and actinic keratosis: preserved normal basal cells in Bowen's disease.

The degree of DNA-instability as revealed by immunohistochemical staining with anti-cytidine antibody after acid hydrolysis (DNA-instability test) has been recently used as a marker of malignancy. This technique was applied to examine 17 skin tissue samples of Bowen's disease, 47 of actinic keratosis, 15 of squamous cell carcinoma, 5 of seborrheic keratosis, and 10 of normal skin. All benign neoplastic cells of seborrheic keratosis and normal epidermal cells were negative. On the other hand, all cancer cells were positive with the DNA-instability test, indicating their malignancy, but all basal cells in Bowen's disease were completely negative. Compatible with this result, the basal cells in Bowen's disease were characteristically normal as evident in other histochemical examinations. Thus, they were negative with p53 immunohistochemistry, with normal signals of chromosome 17 in situ hybridisation and argyrophilic nucleolar organiser region, and showed slightly enhanced proliferative activity as revealed by proliferating cell nuclear antigen immunohistochemistry. Immunohistochemical staining with 34 beta E12 (monoclonal antibody against cytokeratins 1, 5, 10, and 14), which stains all normal epidermal keratinocytes including basal cells, showed that only the basal cells of Bowen's disease stained strongly and homogeneously, while all cancer cells in the upper layers of Bowen's disease and all layers of actinic keratosis were only sporadically or weakly stained. Staining with 34 beta B4 (monoclonal antibody against cytokeratin 1), which recognises the whole epidermis except for the basal layer in the normal epidermis, showed that the basal cells in the Bowen's disease were completely negative, and lower layer cells in the actinic keratosis and upper layer cells in Bowen's disease were only sporadically stained positive, although the superficial layer cells in actinic keratosis stained strongly and homogeneously. Our findings clearly indicate that the basal cells in Bowen's disease are normal. In support of this conclusion, the same cells showed normal morphology on electron microscopy with preserved basement membrane, although the latter was often damaged in actinic keratosis.

Actins↗